Intradialytic parenteral nutrition in hemodialysis patients: Acute and chronic intervention

By Margaret Avery-Lynch, RD, BSc

Abstract
Protein and calorie malnutrition have been encountered more frequently than expected in the hemodialysis patients. Intradialytic parenteral nutrition (IDPN) has been documented to improve nutritional status in hemodialysis patients in both acute and chronic settings (Henrich, 1996). The aim of this study was to support the usage of IDPN in our malnourished hemodialysis patients. Serum concentration of albumin is one of the main indicators of mortality in the dialysis population. The serum albumin concentration for six out of eight of our hemodialysis (HD) patients receiving IDPN increased signicantly. There was a mean increase of 7.0 g/L of plasma albumin for the eight patients assessed. These results demonstrate that IDPN is an effective nutritional intervention for malnourished hemodialysis patients. Key words: intradialytic parenteral nutrition (IDPN), subjective global assessment (SGA)

Hemodialysis patients who have a functional and accessible gastrointestinal tract must be considered rst for oral or enteral feeds. However, patients are chosen if there is inadequate nutritional support from oral and enteral nutrition. This nutritional assessment is completed by a registered dietitian to address the renal patients nutritional requirements. Through this assessment, it is established if their level of protein and calories through their diet is adequate. If the patient requires and tolerates nutritional support, oral supplements such as protein powder and renal supplements are recommended in various doses in an effort to meet patients nutritional needs. Each case is reviewed by the dialysis team. IDPN is primarily reserved for patients with nonfunctioning gastrointestinal tracts. However, for HD patients, the usual barrier to adequate nutrition is an inadequate intake of protein and calories.

Need for IDPN

IDPN is recommended in situations in which patients are not able to consume adequate amounts of uid and calories to maintain normal nutritional status. Patients ability to absorb nutrients may also be compromised. The patient who is critically ill and in a catabolic state may not be able to consume enough food to meet their required energy needs and may require IDPN Table One: The suggested criteria for starting IDPN Low serum albumin levels <30 g/L. Protein catabolic rate/nitrogen balance, nPNA <0.8. Patient consumes >60% orally over an expended period of time >2 weeks Weight loss of 10% to 15% of previously attained dry weight/usual body weight. Functional impairment of the GI tract that prevents sufcient absorption and use of nutrients to maintain weight and strength with a primary diagnosis of malabsorption, gastroparesis, chronic recurrent pancreatitis, liver disease, GI obstruction, radiation enteritis, cancer, inammatory bowel disease or short bowel syndrome. Subjective Global Assessment (SGA) can also be utilized to assess HD patients. A score of C rating can be a factor in determining whether IDPN is used.

Background
The incidence of protein and calorie malnutrition in the end stage renal disease (ESRD) patients in North America is clinically signicant. Mortality and morbidity are directly inuenced by wasting of lean body mass and protein calorie malnutrition. Malnutrition places a signicant economic burden on the health care system. During the mid to latter part of the 1990s, research was devoted to intradialytic parenteral nutrition (IDPN) in health care facilities. These studies strongly suggested that IDPN was an effective therapeutic intervention to correcting malnutrition in ESRD patients (Kopple, 1999). IDPN has been proven to be a convenient and noninvasive therapeutic intervention that provides nutrition during the hemodialysis (HD) procedure. Further randomized studies need to be undertaken to provide more conclusive evidence of its validity as a therapeutic intervention. From October 2001 to October 2002, acute and chronic HD patients at Peterborough Regional Dialysis Program, Ontario, who met the specic criteria for malnutrition were given IDPN. There was a signicantly higher number of patients who needed nutritional support in our dialysis than was expected and the need for immediate and effective nutrition intervention was apparent. The general expectations of surveys concerning nutritional status of maintenance dialysis patients claim that six per cent of patients suffer severe malnutrition (Amber & Kopple, 1998).

Methods
Patients involved in this study are from the Peterborough Regional Dialysis Program. The study included a total of eight acute and chronic hemodialysis patients. Patient dialysis times ranged from 3.5 to 4.0 hours three times a week. Patients received IDPN for durations of 1.5 to 16 months depending on their protein calorie malnutrition state. 30

Margaret Avery-Lynch, RD, BSc, is Renal Dietitian, Regional Dialysis Program, Peterborough, Ontario. Address correspondence to Margaret Avery-Lynch, e-mail: mavery-l@prhc.on.ca Submitted for publication: July 14, 2005. Accepted for publication in revised form: March 12, 2006.

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(Henrich, 1996). It is noted that an assessment of nutritional status should emphasize separating abnormal nutritional parameters from those caused by inammation or uremia. The incidence of malnutrition will continue to rise because of the increase in age and medical complexity of HD patients. The criteria for patient selection for IDPN are outlined in Table One.

Design
This study reports a series of cases in which IDPN was used to improve the nutritional status of patients on HD. All patients who participated in this study were reviewed by the nephrology team (nephrologists, renal dietitian, pharmacist and primary nurse) and recommended for the IDPN. Nutritional parameters such as protein (albumin and nPNA) and weight changes were collected and evaluated. The nephrologist, in consultation with the renal dietitian, ordered IDPN solutions and additives. The pharmacy was notied and reviewed all initial orders and any subsequent adjust-

ments. During each dialysis visit, the patients blood work, weight changes, blood pressures and overall health were assessed both by the nephrologist and dietitian. IDPN solution for patients who did not have diabetes contained 5% amino acid and 25% dextrose. Patients with diabetes received the composition that consisted of 5% amino acid and 16.6% dextrose. Custom electrolytes were integrated into the IDPN solution based on current blood work. There was one patient in the study who had diabetes. Subcutaneous insulin was prescribed for the diabetic patient as part of the IDPN procedure to control hyperglycemia. A blood sugar was drawn pre-, half hour into the infusion and post-dialysis. Initially, the diabetic patients would have their blood sugar levels determined in relationship to carbohydrate intake, insulin regimen and exercise level. On the patients rst day, IDPN blood sugars were taken every hour and the initial dosage of short-acting insulin was given based on one unit of short-acting insulin subcutaneously for every 15g of carbohydrate. Two-hour post-dialysis

Table Two: Summary of the IDPN intervention on acute and chronic HD patients Patient Indications for use Duration of IDPN therapy Serum albumin pre IDPN Weight pre Patient A Male Age: 30 yrs Time on dialysis: 3.0 hrs Patient B Male Age: 78 yrs Time on dialysis: 4.0 hrs Patient C Female Age: 30 yrs Time on dialysis: 3.5 hrs Patient D Male Age: 80 yrs Time on dialysis: 4.0 hrs Patient E Male Age: 75 yrs Time on dialysis: 4.0 hrs Patient F Male Age: 71 yrs Time on dialysis: 4.0 hrs Patient G Male Age: 36 yrs Time on dialysis: 3.5 hrs Patient H Male Age: 74 yrs Time on dialysis: 3.5 hrs Bowel resections Ileostomy SGA C Post surgery Cancer SGA C 11 months 40 g/L 43.0 kg 4 months 33 g/L 54.1 kg Increased catabolic state Pneumonia Restrictive lung disease SGA B Crohns disease SGA B 1.5 months 29 g/L 31.8 kg 4 months 30 g/L 73.0 kg Skin burns Decreased lean body mass SGA C Gastroenteritis Diabetic ulcers Amputation SGA C Increased catabolic state Inammatory state GI ulcer SGA C Burns Increased catabolic state SGA C 5 months 25 g/L 64.2 kg 7 months 26 g/L 84.0 kg 16 months 15 g/L 36 kg 3 months 23 g/L 63 kg Serum albumin post IDPN Weight post 41 g/L 47.5 kg 35 g/L 54.4 kg 45 g/L 31.7 kg 35 g/L 75 kg 33 g/L 63.5 kg 37 g/L 81.9 kg 24 g/L 37.5 kg 28 g/L 62.8 kg Pre 1.1 Post 1.3 Pre 1.1 Post 1.3 Pre 1.0 Post 1.6 Pre 1.1 Post 1.5 Pre 1.1 Post 1.3 Pre .7 Post .9 Pre 1.0 Post 1.7 Pre 1.3 Post 1.5 nPNA

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blood sugar was taken and usual insulin regimen was resumed. The infusion rate started at 150 mL/hr of Travasol and 15 mL/hr of lipids 20%. This rate was increased by 25% from the initial rate each dialysis session until a rate of 250 mL/hr was achieved for Travasol and 35ml/hr maximum for lipids. Factors limiting the rate of infusion were: elevated blood pressures, any systolic blood pressure over 200 mm Hg and diastolic over 100 mm Hg, total ultra ltration volume, not exceeding ve litres, and general tolerance to IDPN. General tolerance was measured by how the patient felt in terms of potential hyperglycemia, muscle cramps, blood pressure control and nausea. Cost limited our use of Travasol to one bag per treatment. A lipid test dose was performed before the rst IDPN infusion to rule out any lymphatic adverse conditions. Post-dialysis, the blood sugar was measured and below 11 mmol/L, 15 g of carbohydrates given orally. A blood sugar less than 11 mmol/L was never documented. IDPN was administered through the medication port on the venous drip chamber of the hemodialysis extracorporeal circuit. IDPN started within ve minutes of starting dialysis and continued until the end of the treatment. Antibiotics, IV iron and blood products were not given simultaneously. If required, IDPN was stopped near the end of dialysis and these treatments provided. The patients on HD were closely monitored for glucose control, hepatic function, and triglyceride levels. During dialysis, they received close blood pressure and blood glucose monitoring. Routine laboratory testing was carried out and results assessed by the medical team.

induced by alterations in dietary intake or nutrient utilization resulting in changes in subcellular, cellular, and/or organ function. This can expose the individual to increased risks of morbidity and mortality. This malnourished state can be reversed by appropriate nutrition support. Nutritional deciency states may be characterized according to specic substances, electrolytes or vitamin deciency states (Henrich, 1996). There are several factors that may contribute to malnutrition in dialysis patients. They are as follows: caloric intake, dialysis procedure, endocrine disorders, uremia and age. Caloric intake Dietary histories reveal lower caloric intakes than the recommended 35 kcal/kg body weight per day (Paskalev, Ikonomov, Hristosov, & Decheva, 2002). Patients with chronic renal disease have increased nausea, vomiting, and may have a decreased appetite due to delayed gastric emptying or other gastrointestinal problems. Depression may also be a contributing factor in a reduced appetite. Dialysis procedure Inadequate dialysis is a contributing factor in causing malnutrition. Studies suggest a positive relationship between protein nitrogen appearance and dialysis adequacy as measured by Kt/V in both hemodialysis and peritoneal dialysis patients (Fenton, Schaubel, Desmeules, Morrison, Mao, Copleston, et al., 1997). There is a loss of nutrients during the dialysis procedure for both biocompatible and bioincompatible membranes. This can induce net protein catabolism due to amino acid losses during the procedure. This loss can amount to 10 g to 13 g of amino acids per treatment, and the patient must catabolize 25 g to 30 g of body protein to compensate for these losses. Between 5 mL and 10 mL of blood may be trapped in the dialyzer at the end of each dialysis and this can account for another 0.6 g to 1.4 g of protein lost per HD procedure (Henrich, 1996). Lofberg et al. (1997) examined the metabolic effect of hemodialysis by measuring muscle ribosome and amino acid content during a single hemodialysis session. Muscle alanine concentration and ribosome content decreased, indicating a fall in capacity of protein synthesis. Amino acid loses in conjunction with protein catabolic effect of hemodialysis may account for the negative nitrogen balance observed in patients on the days of hemodialysis. Endocrine disorders Conditions such as diabetes can cause a higher rate of malnutrition due to specic complications such as gastroparesis, diarrhea, nausea, and bacterial overgrowth in the gut. Mitch, in 2002, reported increased protein degradation in response to hormonal changes due to acidosis. Parathyroid hormone Table Three: Observations Observations Weight change nPNA change Albumin Average 1.13 kg 0.65 7.13 g/L Median 0.8 kg 0.20 6.5 g/L

Results
IDPN therapy was studied from October 2001 to November 2002. Blood chemistries reported in Table Two depict the patients serum albumin and nPNA values. Serum albumin was measured on a weekly basis. Serum albumin levels ranged from 15 g/L to 40 g/L before and 24 g/L to 45 g/L after treatment with IDPN. There was a mean increase of 7 g/L of albumin and a median change of 6.5 g/L. The level of nPNA was calculated before and after IDPN. The nPNA increased signicantly by 0.65 with a median change of 0.20 (see Table Three). Anthropometric measurements including the patients weight were recorded before and after IDPN therapy. The average weight increased by 1.13 kg with a median change of 0.8 kg. This change in weight must be considered in the context of the change in edema. Patients exhibited variable degrees of pitting edema from one to four millimeters. The actual measurements were recorded as mild (1.0 to 2.9 mm depth) and moderate to severe as (3.0 to 4.0 mm). Patients C, E, F and H had severe edema and A, B, D and G had moderate edema. This explains the marginal weight gain since all patients had less edema after their duration of IDPN. The dietitian performed subjective global assessments on each patient. The SGA indicated all patients involved in the study were severely malnourished, but did not merit hospitalization and required extra nutritional intervention.

Discussion
Many studies have established the need for strategies to correct protein energy malnutrition (PEM) in the chronic hemodialysis patient. Malnutrition is dened as a state 32

Patients A,B,D Peripheral Edema Patients C,E,F, Gradation and H and G 4-3.0 millimeters 2.9-1.0 millimeters April June 2006,Volume 16, Issue 2 The CANNT Journal

(PTH) is commonly increased in dialysis patients. Elevated PTH levels may also increase protein wasting and promote negative nitrogen balance. Hyperparathyroidism can act as a catabolic factor that inuences protein metabolism by enhancing amino acid release from muscles. These hormone derangements in uremia can promote decreased protein synthesis and increased protein catabolism (Henrich, 1996). Uremia Muscle protein metabolism is adversely affected by uremic acidosis. Uremia is associated with resistance to a number of anabolic-acting hormones, including insulin, growth hormone (GH), and its major mediator IGF-1. Hyperleptinemia can contribute to a negative energy balance in patients who are uremic. Hyperleptinemia is caused by decreased plasma clearance (speculated by a predisposing loss of renal elimination capacity in correlation with obesity and gender) resulting in down regulation of LEP gene expression (Mitch, 2002; Nordfors et al., 1998). Intercurrent illness such as infections and recent surgical interventions lead to reduced food intake and increased catabolism, which, depletes body stores of protein and fat. Age The average age for the hemodialysis population is increasing and elderly patients are more prone to have or develop comorbid conditions that can interfere with the nutritional state.

The role of SGA Subjective global assessment has been established as a clinical method to help determine the nutritional status of patients on hemodialysis (Fenton et al., 1997). It encompasses a medical history and physical examination that determines the nutritional status of the renal patient. The medical history includes: a review of the patients metabolic changes in the past and present, an extensive dietary recall, gastrointestinal symptoms, activity level, and metabolic demands. The physical examination encompasses a visual examination of subcutaneous fat, muscular wasting, and if the patient has edema or ascites. The patient is rated on a score system from A through C. The scores indicate: A well-nourished, B mildly-moderately malnourished, and C severely malnourished (Baxter, 1994). Jeejeebhoy et al. (1990) found in their research that the composition of somatic muscle tissue is altered with the state of nutrition. They are continuing the research to prove that nutritional support can reverse this muscle tissue erosion (Jeejeebhoy et al., 1994). The SGA is an excellent tool for continuous quality improvement (CQI) measurement. This measurement should be used with objective measures such as biochemical parameters and anthropometric measurements to assess a patients nourished state (Jeejeebhoy, 1990).

Summary
The use of IDPN increased serum albumin levels for all HD patients receiving IDPN. There was a mean increase of 7.0 g/L for all patients. Other studies have reported a 1.5 g/L increase as a signicant improvement in nutritional status. The use of IDPN as a nutritional intervention for patients on hemodialysis has been successful in both acute and chronic settings. One of the most benecial effects of IDPN was an increase in appetite. Henrich, 1996, also noted signicant improvement in food intake while the patient was receiving IDPN. In addition, our study noted a net positive weight gain during IDPN treatment. It is recognized that IDPN is costly and will continue to be reserved for malnourished patients who fail enteral nutrition supplements.

Need for IDPN

IDPN is recommended in situations in which patients are not able to consume adequate amounts of uid and calories to maintain nutritional status. Patients ability to absorb nutrients may also be compromised. The patient who is critically ill and in a catabolic state may not be able to consume enough food to meet their required energy needs and may require IDPN (Henrich, 1996). It is noted that an assessment of nutritional status should emphasize separating abnormal nutritional parameters from those caused by inammation or uremia. The incidence of malnutrition will continue to rise because of the increase in age and medical complexity of patients on HD. The criteria for patient selection for IDPN are outlined in Table Two.

References
Amber, C., & Kopple, J.D. (1998). Nutrition support for patients with renal failure. In American Society for Parental and Enteral Nutrition (ed.), The A.S.P.E.N. Nutrition Support Practice Manual 1998 (pp. 16-1 - 16-11). Silver Spring, MD: A.S.P.E.N. Baxter Healthcare Corporation. (1994). Assessing the nutritional status of dialysis patients using subjective global assessment. Mississauga, ON: Baxter Healthcare Corporation Fenton, S.S., Schaubel, D.E., Desmeules, M., Morrison, H.I., Mao, Y., Copleston, P., Jeffery, J.R., & Kjellstrand, C.M. (1997). Hemodialysis versus peritoneal dialysis: A comparison of adjusted mortality rates. American Journal Kidney Diseases, 30, 334-342. Henrich, W.L. (1996). Malnutrition and intradialytic parenteral nutrition in end-stage renal disease patients. In C.L. Shuler & M. Wolgson (Eds.), Principles and practice of dialysis (2nd ed.). Philadelphia, PA: Lippincott Williams and Wilkins. Jeejeebhoy, K.N., Detsky, A.S., & Baker, J.P. (1990). Assessment of nutritional status. Journal Parenteral and Enteral Nutrition, 14(5 Suppl), 193S-196S. Jeejeebhoy, K.N. (1994). How should we monitor nutritional support: Structure or function? New Horizons, 2(2), 131-138. Kopple, J.D. (1999). Pathophysiology of protein-energy wasting in chronic renal failure. The Journal of Nutrition, 129(1), 247-251. Lofberg, E., Wernerman, J., Anderstam, B., & Bergstrom, J. (1997). Correction of metabolic acidosis in dialysis patients increases branched-chain and total essential amino acid levels in muscle. Clinical Nephrology, 48, 230-237. Mitch, W.E. (2002). Insights into the abnormalities of chronic renal disease attributed to malnutrition. Journal of the American Society of Nephrology, 13, S22-S27. Nordfors, L., Lonnqvist, F., Heimbuger, O., Danielsson, A., Schalling, M., & Steenvinkel, P. (1998). Low leptin gene expression and hyperleptinemia in chronic renal failure. Kidney International, 54(4), 1267-1275. Paskalev, D.N., Ikonomov, V.C., Hristosov, L.Y., & Decheva, L.Y. (2002). Some medical aspects of nutritional therapy in elderly chronic renal failure patients. Dialysis & Transplantation, 31, 607-614.

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